OBJECTIVE Endogenous hypercortisolism predisposes to impaired immune function and infections. To date, however, it is unknown whether there is a subtype-specific pattern in white blood cell (WBC) and WBC differential… Click to show full abstract
OBJECTIVE Endogenous hypercortisolism predisposes to impaired immune function and infections. To date, however, it is unknown whether there is a subtype-specific pattern in white blood cell (WBC) and WBC differential (WBCD) count. METHODS Retrospective monocentric cohort study in patients with overt endogenous Cushing's syndrome (CS) or adrenal incidentalomas and autonomous cortisol secretion (ACS), with WBC/WBCD analysis at initial diagnosis and after biochemical remission. Cut-offs were obtained by receiver operating characteristics analysis. RESULTS 253 patients were analyzed (Cushing´s disease (CD); n=88; ectopic CS (ECS), n=31; cortisol-producing adrenal adenomas (CPA), n=40; ACS, n=45; adrenocortical carcinomas (ACC), n=49). Total leukocytes and neutrophils correlated positively with serum cortisol after 1-mg dexamethasone (r=0.314 and r=0.428), while a negative correlation was observed for lymphocytes and eosinophils (r= -0.374 and r= -0.380) (each p<0.0001). Similar observations were made for 24h-urinary free cortisol. CD and ECS differed in numbers of neutrophils and lymphocytes (p<0.0001) and were well differentiated at a cut-off of 6.1 for the neutrophil/lymphocyte ratio (NLR; sensitivity 90.0%, specificity 89.4%, AUC 0.918). For adrenocorticotropic hormone (ACTH)-independent CS, the best diagnostic outcome was obtained for the discrimination of CPA and ACC at a cut-off of 187.9 for the platelet/lymphocyte ratio (sensitivity 59.6%, specificity 80.6%, AUC 0.713). For ECS, CPA, and CD, neutrophils decreased (delta -47.0%, -29.7%, and -26.2%) and lymphocytes increased (+123.2%, +78.1%, and +17.7%) already 3 months after remission. CONCLUSION Most immune cells correlate with the degree of hypercortisolism and differ among CS subtypes. WBCD changes are already identified three months after remission from endogenous hypercortisolism.
               
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